Abstract

Objective. To investigate the presence and the roles of anti–interleukin‐6 (anti–IL‐6) autoantibodies in rheumatic diseases, and to further elucidate clinical and pathophysiologic significance of anticytokine autoantibodies. Methods. Anti–IL‐6 IgG autoantibodies were measured by the 125I–IL‐6 binding activity of IgG, which was isolated from serum by protein A–Sepharose. Results. Nine of 52 sera (17.3%) from patients with systemic sclerosis (SSc) contained anti–IL‐6 antibodies, whereas only 1.9% of sera from normal subjects and 0–5% of sera from patients with other rheumatic diseases were positive for the antibodies. Moreover, anti–IL‐6 autoantibodies were found predominantly among patients with the limited form of SSc (42.9%), compared with those with the diffuse form (7.9%). Conclusion. Anti–IL‐6 IgG autoantibodies were detected in patients with SSc, particularly those with the limited form of the disease, at a significantly increased frequency compared with normal subjects and patients with other rheumatic diseases. These results suggest that the development of anti–IL‐6 autoantibodies and IL‐6 may have a role in the pathophysiology of SSc.

abstract = "Objective. To investigate the presence and the roles of anti–interleukin‐6 (anti–IL‐6) autoantibodies in rheumatic diseases, and to further elucidate clinical and pathophysiologic significance of anticytokine autoantibodies. Methods. Anti–IL‐6 IgG autoantibodies were measured by the 125I–IL‐6 binding activity of IgG, which was isolated from serum by protein A–Sepharose. Results. Nine of 52 sera (17.3%) from patients with systemic sclerosis (SSc) contained anti–IL‐6 antibodies, whereas only 1.9% of sera from normal subjects and 0–5% of sera from patients with other rheumatic diseases were positive for the antibodies. Moreover, anti–IL‐6 autoantibodies were found predominantly among patients with the limited form of SSc (42.9%), compared with those with the diffuse form (7.9%). Conclusion. Anti–IL‐6 IgG autoantibodies were detected in patients with SSc, particularly those with the limited form of the disease, at a significantly increased frequency compared with normal subjects and patients with other rheumatic diseases. These results suggest that the development of anti–IL‐6 autoantibodies and IL‐6 may have a role in the pathophysiology of SSc.",

N2 - Objective. To investigate the presence and the roles of anti–interleukin‐6 (anti–IL‐6) autoantibodies in rheumatic diseases, and to further elucidate clinical and pathophysiologic significance of anticytokine autoantibodies. Methods. Anti–IL‐6 IgG autoantibodies were measured by the 125I–IL‐6 binding activity of IgG, which was isolated from serum by protein A–Sepharose. Results. Nine of 52 sera (17.3%) from patients with systemic sclerosis (SSc) contained anti–IL‐6 antibodies, whereas only 1.9% of sera from normal subjects and 0–5% of sera from patients with other rheumatic diseases were positive for the antibodies. Moreover, anti–IL‐6 autoantibodies were found predominantly among patients with the limited form of SSc (42.9%), compared with those with the diffuse form (7.9%). Conclusion. Anti–IL‐6 IgG autoantibodies were detected in patients with SSc, particularly those with the limited form of the disease, at a significantly increased frequency compared with normal subjects and patients with other rheumatic diseases. These results suggest that the development of anti–IL‐6 autoantibodies and IL‐6 may have a role in the pathophysiology of SSc.

AB - Objective. To investigate the presence and the roles of anti–interleukin‐6 (anti–IL‐6) autoantibodies in rheumatic diseases, and to further elucidate clinical and pathophysiologic significance of anticytokine autoantibodies. Methods. Anti–IL‐6 IgG autoantibodies were measured by the 125I–IL‐6 binding activity of IgG, which was isolated from serum by protein A–Sepharose. Results. Nine of 52 sera (17.3%) from patients with systemic sclerosis (SSc) contained anti–IL‐6 antibodies, whereas only 1.9% of sera from normal subjects and 0–5% of sera from patients with other rheumatic diseases were positive for the antibodies. Moreover, anti–IL‐6 autoantibodies were found predominantly among patients with the limited form of SSc (42.9%), compared with those with the diffuse form (7.9%). Conclusion. Anti–IL‐6 IgG autoantibodies were detected in patients with SSc, particularly those with the limited form of the disease, at a significantly increased frequency compared with normal subjects and patients with other rheumatic diseases. These results suggest that the development of anti–IL‐6 autoantibodies and IL‐6 may have a role in the pathophysiology of SSc.